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106 Cards in this Set
- Front
- Back
what are the sources of Energy?
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• Proteins
• Fats • Sugars |
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which one is easiest to mobilize?
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sugars
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describe the properties of a charged molecule ie. amino group (-NH4 +)
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Amino Group (-NH4 +): Charged, more soluble, attracted to water
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describe the properties of a uncharged molecule ie. acid group (-COOH)
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Acid Group (-COOH): Uncharged, crosses membranes, reflection coefficient closer to zero, more
bioavailable |
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Buffers:
what is the intracellular buffer?, extracellular buffer and the best buffer? |
• Intracellular: Protein (RBC's=hemoglobin)
• Extracellular: Bicarbonate • Best Buffer: Histidine (pK = 6.0, sidechain closest to pH=7.4) |
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what is an Amino acids:
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have an NH3+ and a COOH
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Proline: where is it more abundant?
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imino acid ⇨ think kinks, twists, bends, turns (Ex: GI, hair, blood vessels)
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Dissociate
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=> take H + away!
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Bioavailable
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=> neutral, can cross membranes, fat soluble
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Soluble
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=>charged or polar, water soluble (Sulphur, Oxygen, Nitrogen)
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Acids
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pKa<7, likes to give up hydrogen ions, dissociates early
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Base:
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pKa>7, likes to accept hydrogen ions, dissociates late
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pKa 1-3
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Strong acid
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pKa 4-7
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Weak acid:
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pKa 7-9
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Weak base:
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pKa 10-14
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Strong base:
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pKa of 4-9
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can be a weak acid or weak base
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what happens when an acid dissociate:
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gains negative charge, more soluble, less bioavailable
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what happens when a bases dissociate:
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loses a positive charge, less soluble, more bioavailable
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Henderson-Hasselbach Equation
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pH= pK -log Base/ Acid
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what does it mean when pH= pK
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Half acid and half base
• 50% dissociated • 50% soluble • 50% bioavailable • 50% reflection coefficient close to 1 • 50% reflection coefficient close to 0 • 50% crosses BBB (bioavailable) • 50% metabolized by liver (bioavailable) |
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pH: pK+2
Dissociated = Water Soluble: Bioavailable=Fat Soluble: for both acid/ base pK+2 99% 1% |
Dissociated = Water Soluble/
Bioavailable=Fat Soluble 99%/1% (acid), 1%/99% |
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pH: pK. + 1
Dissociated = Water Soluble: Bioavailable=Fat Soluble: |
Dissociated = Water Soluble/
Bioavailable=Fat Soluble 90%/10% (acid), 10%/90% (base) |
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pH:pK
Dissociated = Water Soluble: Bioavailable=Fat Soluble: |
Dissociated = Water Soluble:
Bioavailable=Fat Soluble |
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pH: pK. - 1
Dissociated = Water Soluble: Bioavailable=Fat Soluble: |
Dissociated = Water Soluble/
Bioavailable=Fat Soluble 50% "Best Buffer" 50% |
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pH: pK.- 2
Dissociated = Water Soluble: Bioavailable=Fat Soluble: |
Dissociated = Water Soluble/
Bioavailable=Fat Soluble 1%/99% (acid), base 99%/1% (base) |
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Rules to keep molecules neutral (bioavailable):
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• To absorb more acid, place in a stronger acid
• To absorb more base, place in a stronger base |
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Common Acids
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NH4Cl, ASA, Barbiturates, Myoglobin, Juice, Coke
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Common Bases
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Bicarb, Amphetamines, Baking soda, Activated charcoal, Milk
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what are the anti-inflammatories?
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Acetaminophen
NSAIDs: COX inhibitors COX-2 Inhibitors |
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Acetaminophen: MOA, SE and toxicity tx
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works at hypothalamus to decrease temp
• Liver toxicity: microsteatosis (highest levels in first 4 hours) • Tx: N-acetylcystirte (absorbs free radicals) |
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NSAIDs: SE and what are the two types of NSAIDs and location
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COX inhibitors => GI bleeding, interstitial nephritis
COX-1: on gut tissue COX-2: on endothelial tissue |
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what are the COX-1 inhibitors
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Indomethacin
Phenylbutazone Ketorolac Baclofen Cyclobenzaprine Naproxen Ibuprofen asa |
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Indomethacin
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most potent => RTA, closes PDA, tx gout
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Phenylbutazone
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2nd most potent
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Ketorolac
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morphine-like, use w / drug addicts
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Baclofen
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tx back pain (GABA-ergic effect)
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Cyclobenzaprine
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anti-cholinergic effects (hot, dry skill)
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Naproxen
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tx dysmenorrhea
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Ibuprofen
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OTG
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asa
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acetylates COX-1/2 irreversibly=> most effective platelet inhibitor
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why can we use aspirin in asthma patients
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induces asthma sx because ⇧LT by blocking COX.
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don't use aspirin w/ hyperthyroid pts?
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displaces T4 from TBG
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why can't gout patients use aspirin?
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⇩urate excretion.
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COX-2 Inhibitors advantage
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decreased GI irritation
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what are the cox 2 inhibitors
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• Celecoxib
• Rofecoxib • Valdecoxib • Meloxicam |
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Platelet Haptens:
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• Quinidine}
• ASA (>81mg} • Heparin |
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which cox 2 inhibitor has sulfur?
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Celecoxib
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which cox 2 inhibitor was taken of the maket due to stroke increase?
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Rofecoxib
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which cox 2 inhibitor does not have sulfur?
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Valdecoxib
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ASA Toxicity
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1) Resp Alkalosis (⇧RR)
2) Metabolic Acidosis (uncouples OP) 3) Mixed Acidosis (⇧GABA) |
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Sulfur Side Effects: CI
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don't give to pregnant women
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Sulfur Side Effects
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Anaphylaxis
Rash Interstitial nephritis Hemolytic anemia Met-Hemoglobin Displaces stuff off of albumin Kidney stones |
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what are the Street Drugs: Uppers? and what effect do they have on the eyes?
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dilated pupils
PCP LSD Amphetamines Nicotine Ecstasy |
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PCP "angel dust":
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blocks NMDAr =>powerfully violent, nystagmus, ⇧CPK, ⇧SGOP
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LSD "acid, trips":
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5-HT agonist => laid back=> colorful hallucinating
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Amphetamines "speed, ecstasy, ice=smoked":
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hyperactivity, vertical nystagmus
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Nicotine
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⇩DA reuptake =>agitation, cotinine metabolites in urine
(Tx: Bupropion) |
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Ecstasy
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very thirsty
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Cocaine
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"coke, snow, crack=smoked": ⇩DA reuptake
o Condescending, grandiose, big pupils, formication, HTN, ⇧TPR Fetus: ⇩limbs, VSD, brain bleed, placenta abruptio |
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Cocaine Chest Pressure Tx:
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1) BZ (⇩HR/BP)
2) Nitrate» (⇩vasospasm) 3) Aspirin (⇩thrombi) |
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Cocaine HTN Tx:
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1) Lorazepam (anxiolytic)
2) Phentolamine (⇩BP) 3) Avoid β-blockers |
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Opiod Withdrawal Tx:
neonates adults |
Neonates: Paregori"
Adults: Clonidine /Methadone |
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Cocaine Rhabdomyolysis Tx:
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1) IVF
2) Bicarbonate (keep Mb soluble) |
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what are the street downers:
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Marijuana
Heroin Alcohol |
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Heroin
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"smack, ****": inhibits AC => constipation, pinpoint pupils
(Tx: naloxone, Methadone) |
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Alcohol
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=> ataxia, euphoria, slurred speech, ⇧GGT, AST>ALT
(Tx: thiamine/glucose.+ BZ) |
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Marijuana
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"dope, grass, weed, pot": Δ-9 THC => munchies, red eyes, impaired time orientation
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Isoelectric Point (pi)
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pH at which there is no net charge (pi= (pK1 + pK2)/2)
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Zwitterions
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have a negative carboxy and positive amino end
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Cathode
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where cations go, the negative electrode
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Anode
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where anions go, the positive electrode
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Acidic aa
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Asp, Glu
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Basic aa
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Lys, Arg
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what enzyme cut basic aa?
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Trypsin cuts basic aa
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Sulfur aa
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Cys, Met
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what enzyme cuts aa that have sulfur in them?
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β-ME cuts
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0-Bonds aa?
significance of Tyr? |
Ser, Thr, Tyr
Tyr makes catecholamines, melanin |
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N-Bonds aa?
significance? |
Asn, Gln
Acid hydrolysis denatures |
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Branched aa?
significance? |
Leu, Ile, Val
Maple syrup urine disease |
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what are Aromatic aa?
what enzyme cuts them? |
Phe, Tyr, Trp
Chymotrypsin cuts "bulky word/ rings" |
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Smallest aa?
significance? |
Gly
Spinal cord inhibitor |
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NMDA pathway excitatory aa?
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Asp
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Kinky (Imino)
significance? |
Pro
Yellow on Nurhydrin reaction |
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Active sites aa
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Ser
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Ketogenic
significance |
Lys, Leu
Broken down to Acetyl CoA |
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Glucogenic +Ketogenic
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Phe, Iso, Thr, Trp
(Bulky) "Mr. PITT never Tyrs" |
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who should avoid Ketogenic diet
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Diabetes I
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who should avoid glucogenic diet
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Diabetes II
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Reasons for Dialysis:
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• Symptomatic Uremia
• Symptomatic Acidosis • Hyperkalemia |
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Disulfide Bonds:
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"PIGI"
• PRL • Insulin • GH • lnhibin |
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what does Increased GABA levels lead to?
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bradycardia, lethargy,
constipation, impotence, and memory loss. This means that anything or any disease that increases acidosis, urea, or ammonia will lead to an increase in GABA which will slow everything down. NH3 + H+ ⇨ NH4+ αKG ⇨ Glu ⇨ GABA |
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Essential FA (must eat 'em):
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Linolenic
Linoleic ⇨ AA ⇨ PG |
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Essential Amino Acids: you gotta eat 'em:
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"PVT TIM HALL"
Phe, Val, Trp ⇨5HT, Thr, Ile, Met ⇨Cys, His, Arg, Leu, Lys |
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Newborn screening:
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"Please Check Before Going Home"
PKY (Guthrie test) Congenital adrenal hyperplsia Biotiniase deficiency Galactosemia Hypothyroidism |
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Energy Utilization:
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1) Plasma Glucose: 2-4 hr
2) Liver Glycogen: 24-48 hr 3) Proteolysis for Gluconeogenesis 4) Fats for Lipolysis 5) Ketones for Ketogenesis |
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AA Disorders (AD):
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Met + ATP ⇨ SAM ⇨ Homocysteine ⇨ Cys + propionylCoA ⇨ MMCoA
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PKU
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Phe ⇨ Tyr ⇨ DOPA ⇨ DA ⇨ NE ⇨ Epi
DOPA ⇨T4 and Melanin (albinism) |
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Phenylketonuria:
presentation and test |
No Phe ⇨ Tyr (via Phe-OHase)
• Mental retardation (can't make DA, NE, Epi) • Pale, blond, blue eyes (no melanin) • Musty odor (phenylacetate + phenylpyruvate) • Nutrasweet sensitivity (Phe) • Sclerodermatous plaques • Test: Guthrie test (bacterial inhibition assay) |
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Albinism
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No Tyr ⇨ Melanin (via Tyrosinase)
• Paleness, predisposed to skin cancer |
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Vitiligo:
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• Anti-melanocyte AB
• Pale, predisposed to skin cancer • Ex: Michael Jackson. |
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Alkaptonuria "Ochronosis":
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• Kids w / osteoarthritis (black tendons), black urine
• Homogentisic acid oxidase deficiency |
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Maple Syrup Urine Disease:
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"Life is sweet, so LIV it up!"
Defective renal transport of branced aa (Leu, Iso, Val) => aa leak out |
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Homocystenuria: mode of inheritance, pathogenesis
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Homocysteinuria (AD): No homocysteine ⇨Cys⇨(via cystathione synthase)
>Defective amino acid transport |
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Homocystenuria is caused by?
presentation |
>Caused by high fat diet: increased Met levels
>Dislocated lens from top " >Recurrent kidney stones |
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what are the 4 Amino Acids show up in Urine in homocystenuria?
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Defective amino acid transport "COLA"
• cystine stones⇦ + urine CN Nitroprusside • ornithine • Lysine - basic aa • Arginine - basic aa |